[Downloaded free from http://www.tropicalparasitology.org on Friday, August 28, 2020, IP: 46.163.61.

4]

Letter to Editor

sided facial nerve palsy of lower motor neuron lesion

Plasmodium vivax malaria type was noted [Figure 1]. Rest of the neurological
with isolated facial nerve palsy: examination was noncontributory. Examination of the
ears, nose and throat as well as rest of the systemic
A rare association examination showed no abnormality. Cerebrospinal
fluid (CSF) analysis showed glucose level of 56 mg/
dl and protein of 37 mg/dl with cell count of 5 white
Sir, blood cell/mm3 (all lymphocytes). Routine laboratory
tests including complete blood counts, liver and renal
Malaria is probably the most important tropical function tests, serum electrolytes were within normal
parasitic disease in the world causing millions of deaths range; urine, stool, and blood cultures yielded no
worldwide, especially in third world countries and growth. Hepatitis viruses serology were negative.
mainly among children. Neurological manifestations Abdominal ultrasonography and chest X‑ray revealed
of malaria usually appear in Plasmodium falciparum
no abnormality. Malaria parasite antigen test for P. vivax
malaria and may include cerebellar ataxia, and Guillain–
was positive with asexual forms of the parasite noted
Barre syndrome, raised intra‑cranial tension, acute
on slide smear examination. P. falciparum was not found
transverse myelitis, radiculopathies, cerebral coma.
on antigen testings or slide smear examination. Cranial
Neurological manifestations in Plasmodium vivax are
magnetic resonance imaging (MRI) scan revealed no
comparatively less common and isolated cranial palsy
vascular insult or demyelination in brainstem or any
is extremely rare. Literature on seventh cranial nerve
meningeal enhancement or frontotemporal abnormal
palsy as sole neurological manifestation of falciparum
intensity [Figures 2 and 3 ]. He was treated with
malaria is extremely scanty. To the best of the author’s
oral paracetamol and adequate oral fluids and oral
knowledge, only one case of facial palsy in vivax malaria
chloroquine in recommended dosages  (25  mg/kg
is reported before.[1] The author here presents a case of
over 3 days) followed by oral primaquine (0.25 mg/kg
a 50‑year‑old male who presented with left sided lower
motor type of facial nerve palsy 5 days after developing daily for 14  days) after glucose 6 phosphate assays.
clinical malaria. Symptoms of malaria subsided within Symptoms of fever and headache subsided within 36 h.
48  h following administration of chloroquine but He was discharged after 4  days in stable condition,
complete facial nerve recovery required 7 more days. but complete recovery of the facial nerve took another
The objective of this report is to draw the attention 7 days.
of clinicians especially in developing countries like
India and Sub‑Saharan nations to keep in mind this Diabetes mellitus, chronic suppurative otitis media,
uncommon manifestation of malaria, though the exact meningitis, mumps parotitis, human immunodeficiency
patho‑physiological mechanism remains obscure. virus and intra‑cranial space occupying lesions are
known causes of facial nerve palsy . However, the
A 50‑year‑old nondiabetic, nonhypertensive male mechanism underlying facial nerve palsy in malaria
was admitted with a history of severe headache and caused by P. vivax is unclear. Sim et al. reported facial
high‑grade intermittent fever for last 3 days. Clinical diplegia in a 20‑year‑old boy infected with P. vivax in
examination revealed a fully conscious and alert patient Korea while Duque et  al. reported bilateral 6th cranial
with axillary temperature of 39°C and normal vitals nerve palsy caused by P. falciparum in a 14‑year‑old
except tachycardia. No lymphadenopathy was noted Caucasian living in a democratic republic of Congo.[1,2] In
anywhere in the body. Mild nontender splenomegaly recent years, in a case‑series involving 10 children with
was noted although liver was not palpable. Two days facial palsy, Folayan et al. found malarial association in
after admission, he noticed that he was troubled by 4 cases. They observed complete resolution of the facial
dribbling of saliva from the left angle of his mouth palsy in all 4 cases with resolution of malaria. However,
and his mouth had become deviated to the right. There out of the 4 cases, 2 patients also had concomitant mumps
was no antecedent head injury, no convulsion, altered infection leading to uncertainty over the role of malarial
sensorium, respiratory tract infection, rash on the infection as an etiology behind facial palsy in these
trunk or behind the ear, acute or chronic ear discharge patients, and the researchers felt that a further study is
or any associated speech or hearing impairment. warranted to elucidate the relevant patho‑physiology of
There was no history of vomiting or diarrhea. Left malaria associated facial palsy.[3]

Tropical Parasitology 33 Jan 2015 | Volume 5 | Issue 1 |

[Downloaded free from http://www.tropicalparasitology.org on Friday, August 28, 2020, IP: 46.163.61.4]

Letter to Editor

nervosum, which may lead to temporary demyelination

and recovery after disappearance of the parasitemia
and establishment of normal blood flow in the vasa
nervosum. Although P. falciparum is known for such
pathology, whether P. vivax possesses the same
mechanism is debatable. In the malaria  (of both
falciparum and vivax types), asexual stage infections
are accompanied by the release of cytokines and
other immunological mediators leading to a scenario
mimicking Guillain–Barre syndrome.[4] It is likely that
these immunological mediators may have caused the
demyelination in our patient giving rise to Guillain–
Barre like syndrome affecting only the facial nerve.
However, no serologic test could be done for the
purpose of isolating such antibodies against neuronal
Figure 1: Left sided lower motor neuron type facial nerve palsy tissues for want of facility. Possibility is there that the
facial palsy may be due to local effect of the parasites
on the facial nerve since the paralysis is of the lower
motor neuron type. However, this is debatable as it is
not known whether facial nerve can be directly affected
by P. falciparum or P. vivax.

In the index case, meningitis, diabetes mellitus and

intra‑cranial lesions were reasonably excluded by
CSF analysis, MRI scan and blood sugar estimation.
Herpes zoster affectation of the 7th cranial nerve within
the mastoid bone is a common cause of facial palsy.
However, this is usually associated with vesicular rash
behind or in the ear.[5] Our patient had no evidence of
such rash clinically, though viral serology would have
been useful to rule completely out the infection that
was not done for want of facilities. The only evidence
Figure 2: Normal finding at the level of pons in T2 flair weighted brain of the cause of fever and facial nerve paralysis in
magnetic resonance imaging axial view this patient is P. vivax antigen test positivity and
slide smear demonstration of the asexual forms of
the parasite. The temporal relationship of malaria
and facial nerve palsy and resolution of facial palsy
following resolution of malaria suggests the malaria as
the most possible etiology behind this facial palsy. It
can be reasonably concluded that clinicians practicing
in malarial endemic areas should remember this
rare and unusual manifestation of malaria before
embarking upon more sophisticated tests for finding
the etiology behind facial palsy in proven cases of
malaria.

Subrata Chakrabarti
Department of General Medicine, IPGMER, Kolkata, West Bengal, India.
E‑mail: [email protected]
REFERENCES
Figure 3: No basal exudate or vascular insult or demyelination in T2
flair weighted brain magnetic resonance imaging sagittal section 1. Sim JE, Choi YC, Kim WJ. Facial diplegia in Plasmodium
vivax malaria. J Clin Neurol 2010;6:102‑3.
2. Duque V, Seixas D, Ventura C, Da Cunha S,
It has been postulated that malarial parasite may Meliço‑Silvestre A. Plasmodium falciparum malaria,
damage the peripheral nerves by vascular occlusion, bilateral sixth cranial nerve palsy and delayed cerebellar
thus causing anoxic stagnation involving the vasa ataxia. J Infect Dev Ctries 2012;6:290‑4.

Jan 2015 | Volume 5 | Issue 1 | 34 Tropical Parasitology

[Downloaded free from http://www.tropicalparasitology.org on Friday, August 28, 2020, IP: 46.163.61.4]

Letter to Editor

3. Folayan MO, Arobieke RI, Eziyi E, Oyetola EO, Elusiyan J. Access this article online
Facial nerve palsy: Analysis of cases reported in children Quick Response Code:
in a suburban hospital in Nigeria. Niger J Clin Pract Website:
2014;17:23‑7. www.tropicalparasitology.org
4. Wijesundere A. Guillain‑Barré syndrome in Plasmodium
falciparum malaria. Postgrad Med J 1992;68:376‑7.
DOI:
5. Okike CO, Ezeonu CT, Onyire BN, Manyike PC. Facial
nerve palsy: An unusual feature of Plasmodium 10.4103/2229-5070.145596
falciparum. Paediatr Health 2013;1:1.
DOA: 08-09-2014 DOP: ***

Tropical Parasitology 35 Jan 2015 | Volume 5 | Issue 1 |